In this project, we have been studying developmental adaptations of Trypanosoma cruzi to the vertebrate host and, in particular, surface membrane changes occurring during the morphogenesis of epimastigotes (vector stage) to trypomastigotes (verbetrate stage). Using a radioimmunoassay, we analyzed the loss occurring during this transformation of a carbohydrate epitope recognized by a monoclonal antibody (29.26). Over half of the loss took place while the parasites were still in the epimastigote stage. This decrease in antigenic activity could be mimicked by elevation of cultured epimastigotes from 26 C to 37 C. The remaining loss in the antigen binding activity occurred during the actual morphologic transformation of epimastigotes into trypomastigotes. Surface labeling studies confirmed that this loss in reactivity was due to the disappearance from the membrane of the entire 72,000 MW molecule recognized by 29.26 antibody. In a related study, strains and clones of T. cruzi were screened for their reactivity with 29.26 antibody. Approximately half of the isolates tested failed to react in the radioimmunoassay. Positive and negative clones were identified within one strain. Surface labeling studies have suggested that this divergence in the reactivity of epimastigotes with 29.26 results in the case of some isolates from membrane changes rendering the epitope cryptic, in the case of other isolates from structural changes in the 72K molecule, and in the case of one isolate from absence of the entire 72K molecule.